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17 Cards in this Set
- Front
- Back
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Outline the group of drugs that are used to treat hyperglycaemia in diabetes mellitus |
Insulin Sulfonylureas Biguanides Thiazolidinediones Alpha glucosidase inhibitors |
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Describe the different types of insulin used in the routine management of type I diabetes |
Rapid and short acting Clear solution, neutral pH Insulin lispro/neutral/actrapid Intermediate acting Turbid solution, neutral pH protamine in phosphate buffer to prolong action Long acting Clear solution, slow onset, prolonged action Daily admin mimics basal insulin secretion Insulin glargine |
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How are these properties used to achieve optimum glycaemic control? |
Tight glycaemic control is maintained by a combination of insulins w/ different durations of action. Aim to replace basal insulin requirements 50% and meal requirements 50% |
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What type of insulin is used for IV infusion and why? |
Short acting regular soluble insulin as it imm dissociates and more precisely delivered |
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What pharmacological methods are used to optimise blood sugar control when administering insulin? |
Titration of dose to BSL Pharmacological manipulation of human insulin molecule, ie. rapid, intermediate + long acting Combination of insulins with different duration of action Continuous subcut insulin infusion devices |
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What are the complications of insulin administration? |
Hypoglycaemia Insulin allergy Immune insulin resistance Lipodystrophy at injection sites |
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Contrast the mechanism of actions of sulfonylureas and biguanides? |
Sulfonylureas: Increase insulin release from pancreas Reduction of serum glucagon Biguanide: Not dependent on functioning pancreatic B cells Mech unclear, reduce hepatic gluconeogenesis May directly stimulate glycolysis in tissues Slow glucose absorption GIT |
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Describe the pharmacokinetics of metformin? |
well absorbed orally Not protein bound Not metabolised Excreted unchanged in kidney T1/2 1.5 - 3hrs |
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Outline some common side effects of metformin |
GIT s/e Lactic acidosis - esp in pts renal disease, ETOH |
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What class of drug is gliclazide? |
Sulphonylurea |
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Describe the mechanism of action of sulfonylureas |
Stimulates insulin secretion from functional pancreatic beta cells - Binding of sulfonylureas to receptor inhibits K efflux, leads to extracellular depolarisation + opening voltage gated Ca channels - Ca influx causes release of preformed insulin |
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What are the pharmacokinetic properties of gliclazide? |
Well absorbed orally Bioavailability 80% Plasma protein bound Metabolised liver to inactive metabolites Excreted in kidney t1/2 12hrs |
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What are the potential adverse effects of gliclazide? |
Hypoglycaemia GI upset: n/v/pain/diarrhoea Rash |
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Describe the mechanism of action of corticosteroids at a cellular level? |
Most of effect due to widely distributed glucocorticoid receptors Steroid enters cell as free molecule Binds to intracellular receptor bound to a stabilising protein (heat shock protein) Steroid-receptor complex actively transported into nucleus, where binds to glucocorticoid receptor elements on the gene Interacts w/ DNA and alters transcription, results in mRNA exported to cytoplasm for protein production and final hormone response |
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How can corticosteroids be classified? |
Anti-inflammatory activity - Potency: hydrocortisone 1, pred 5, dex 30 Duration of action - dex long acting, hydrocort short Mineralocorticoid activity - Fludrocortisone vs dex Topical vs non-topical |
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What are the effects of hydrocortisone? |
Mediated by glucocorticoid receptors - Metabolic - Permissive effect on vasc reactivity Nadr/Adr - Anti-inflam/autoimmune |
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What are the side effects of corticosteroid use? |
Short term: < 2wks - insomnia, behavioural changes, hyperglycaemia, pancreatitis/peptic ulcer Long term: - Cushing's syndrome: moon faces, fat redistribution, wt gain, striae - Hyperglycaemia/DM - Adrenal suppression - Immunosuppression - osteoporosis, avasc necrosis/myopathy - Na retention/oedema - Poor wound healing - Psychiatric - hypomania, acute psychosis, depression |
